Renal Effects of Prostaglandins and Clinical Adverse Effects of Nonsteroidal Anti-Inflammatory Agents

Garella, Serafino; Matarese, Richard A.

doi:10.1097/00005792-198405000-00003

Cited by 209 publications

(62 citation statements)

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“…Prostaglandin E2 is a potent renal medullary vasodilator but under normal conditions it does not play an important role in the maintenance of renal blood flow. However, a deficiency in the presence of reduced perfusion or volume or sodium depletion may cause a fall in the glomerular filtration rate and renal blood flow (Garella & Matarese, 1984). Neither paracetamol nor indomethacin reduced the glomerular filtration rate or renal blood flow as measured by the renal clearances of inulin, creatinine and PAH.…”

Section: Urine Volume and Osmolalitymentioning

confidence: 97%

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The comparative effects of paracetamol and indomethacin on renal function in healthy female volunteers.

Prescott

Mattison

Menzies

et al. 1990

Brit J Clinical Pharma

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1 Renal function was assessed in 10 healthy female volunteers during administration of placebo, paracetamol (acetaminophen) (4.0 g daily) and indomethacin (150 mg daily) for 3 days under conditions of controlled sodium and fluid intake. 2 Paracetamol and indomethacin had no significant effect on the glomerular filtration rate and effective renal plasma flow as measured by the renal clearances of inulin, creatinine and p-aminohippurate (PAH). 3 Compared with placebo, paracetamol reduced the mean urinary excretion of prostaglandin E2 by 43% on the second day and 58% on the third treatment day (P < 0.01). With indomethacin the corresponding reductions were 73 and 80%. Paracetamol and indomethacin had much less effect on the excretion of prostaglandin 6-keto Fia, and a significant decrease was observed only on the third day. 4 The decreased urinary excretion of prostaglandin E2, produced by paracetamol was associated with a reduction in sodium excretion of more than 50% (P < 0.01) and delay in the onset of diuresis following an acute water load. 5 The renal effects of paracetamol and indomethacin appear to differ. Although indomethacin reduced prostaglandin excretion more than paracetamol it had a similar effect on sodium excretion and less initial antidiuretic action. Unlike paracetamol, indomethacin also reduced basal plasma renin activity. 6 Paracetamol reduced the total body clearance of PAH and increased its plasma halflife. This effect could be attributed to inhibition of the acetylation of PAH by paracetamol. 7 In normal use paracetamol does not appear to have the adverse renal effects associated with the non-steroidal anti-inflammatory analgesics and further studies are required to establish the clinical significance of these findings.

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Section: Urine Volume and Osmolalitymentioning

confidence: 97%

“…The adverse effects of aspirin and the non-oedema, hyponatraemia, hyperkalaemia and steroidal anti-inflammatory drugs on renal func-antagonism of the effects of diuretics and antition have attracted considerable attention over hypertensive agents (Garella & Matarese, 1984; the years. By inhibiting renal prostaglandin Oates, 1988).…”

Section: Introductionmentioning

confidence: 99%

The comparative effects of paracetamol and indomethacin on renal function in healthy female volunteers.

Prescott

Mattison

Menzies

et al. 1990

Brit J Clinical Pharma

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“…Naproxen is highly effective at inhibiting renal PGs, resulting in decreased renal blood flow (Garella and Matarese 1984). Specific renal consequences include decreased glomerular filtration rate, increased vasopressin, increased sodium retention, and decreased Uvol.…”

Section: Fluid and Electrolyte Balancementioning

confidence: 99%

“…Numerous PG subsets are responsible for not only promoting pain and inflammation, but also maintaining blood pressure (BP), plasma volume, and renal function. Less imperative in normal healthy individuals, PGs are critical in maintaining homeostasis during altered cardiovascular states (e.g., hypotension) or altered fluid regulation (e.g., hypovolemia and sodium imbalance) (Garella and Matarese 1984)-common conditions experienced during physical activity. Inhibiting PGs can perpetuate altered cardiovascular and renal function, potentially leading to serious fluid and electrolyte imbalances (e.g., hyponatremia and hypertension) or even acute renal failure (Garella and Matarese 1984;Rosner and Kirven 2007).…”

Section: Introductionmentioning

confidence: 99%

Effects of a 24-h naproxen dose on hydration and electrolyte measures during moderate-intensity cycling in the heat

Emerson

Torres-McGehee

Davis

et al. 2017

FACETS

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Few controlled laboratory studies have examined the negative effects non-steroidal anti-inflammatory drugs can have on fluid-electrolyte balance during exercise. Our objective was to determine whether a 24-h naproxen dose negatively affected hydration and electrolyte measures before, during, and 3 h after 90 min of cycling in a hot or ambient environment. Using a double blind, randomized and counterbalanced cross-over design, 11 volunteers (six male, five female) completed four trials, with conditions as follows: (1) placebo and ambient, (2) placebo and heat, (3) naproxen and ambient, and (4) naproxen and heat. We found no statistically significant differences among experimental conditions for any dependent measures. Though not statistically significant, mean fluid volume was higher and urine volume was lower during naproxen trials compared with placebos. Mean aggregate plasma sodium was <135 mmol/L at all time points and did not significantly change over time. Overall plasma potassium significantly increased pre-(3.9 ± 0.4) to post-exercise (4.2 ± 0.4 mmol/L, p = 0.02). In conclusion, an acute naproxen dose did not significantly alter hydration-electrolyte balance. The trend for naproxen to increase fluid volume and decrease urine volume suggests the start of fluid retention, which should concern individuals at risk for hyponatremia or with pre-existing cardiovascular conditions.

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“…The first mechanism is inhibition of production of prostaglandins. 5 Prostaglandins are not only humoral mediators of the inflammatory response; they are also powerful renal vasodilators, particularly prostaglandins PGD 2 and PGE 2 .…”

Section: Discussionmentioning

confidence: 99%

Glafenine-Induced Acute Renal Failure: Report of Two Cases

1988

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RK Gupta, JVD Meulen, KV Johny, Glafenine-Induced Acute Renal Failure: Report of Two Cases. 1988; 8(4): 288-289 GLAFENINE, an anthrinilic acid derivate, is an analgesic with good gastric tolerance. It is not marketed in the United Kingdom and the United States of America, which may be the reason why an English standard book on drugs mentions only its analgesic effect 1 and an American standard book on therapeutics does not mention the drug at all.2 Only once the drug is mentioned as a nonsteroidal anti-inflammatory drug in the American literature. However, since 1972 several cases of reversible acute renal failure after the ingestion of supratherapeutic doses have been reported in France, where the drug is particularly popular. 4 Because glafenine is commercially available in the Middle East, two cases of acute renal failure following the consumption of an overdose of glafenine are reported. Case Reports Case 1A 21-year-old man had generalized abdominal pain, vomiting, and scanty urine for about 2 days. These complaints had started a few hours after he had consumed 20 200-mg tablets of glafenine. He was first treated elsewhere with antispasmodics and intravenous fluid and was then referred to the Nephrology Unit of the Mubarak Al-Kabeer Hospital because of the oliguria.At admission he looked ill, but not dehydrated. His heart rate was 100 beats per minute, blood pressure was 150/90 mm Hg, and temperature was 37.5°C. Urinary bladder was not felt, and further physical examination was noncontributory. Abdominal ultrasound showed normal-sized kidneys with no evidence of obstruction.He remained oliguric for 6 days. Blood urea and serum creatinine levels, elevatedc on admission, rose to 37.2 mmol/L and 1193 µmol/L, respectively. On the third hospital day, hemodialysis was started and repeated twice thereafter. On the sixth day of admission a percutaneous renal biopsy was performed. It showed normal histologic findings and no signs of interstitial nephritis. Seven days after admission his urine output started to improve. At discharge his blood urea and serum creatinine levels were 7.6 mmol/L and 140 µmol/L, respectively. The patient was subsequently followed up regularly, and 6 months after discharge, normal renal function continues. Case 2A 17-year-old girl had vomiting and mild epigastric pain. The pain was localized and was not associated with altered bowel habits. She had not noticed any decrease in urine output. Five or 6 hours prior to admission the patient was alleged to have consumed 17 200-mg tablets of glafenine for headache and nervous tension. She had not noticed any decrease in urine output.At admission she was afebrile, her heart rate was 80 beats per minute, and blood pressure was 110/70 mm Hg. The systemic clinical examination did not reveal any abnormality, particularly signs of dehydration.Abdominal ultrasound revealed normal-sized kidneys with no evidence of obstruction. On the second hospital day blood urea and serum creatinine levels, elevated on admission, rose to 14.8 mmol/L and 308 µmol/L, re...

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Renal Effects of Prostaglandins and Clinical Adverse Effects of Nonsteroidal Anti-Inflammatory Agents

Cited by 209 publications

References 0 publications

The comparative effects of paracetamol and indomethacin on renal function in healthy female volunteers.

The comparative effects of paracetamol and indomethacin on renal function in healthy female volunteers.

Effects of a 24-h naproxen dose on hydration and electrolyte measures during moderate-intensity cycling in the heat

Glafenine-Induced Acute Renal Failure: Report of Two Cases

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